Mouse studies suggest Treg
cells that lose expression of FOXP3 and become Th17 cells can
contribute to arthritis and could provide a useful biomarker to aid arthritis
drug development. In a mouse model of collagen-induced arthritis, a
population of Foxp3+ T cells lost Foxp3 expression, converted
into Th17 cells and led to joint swelling and bone destruction. In cell
culture, the conversion into Th17 cells depended on the presence of synovial
fibroblasts and the production of Il-6. Next steps include
identifying a molecular signature specific to Foxp3-depleted T cells that
could serve as a biomarker or reveal potential therapeutic targets.

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